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Glia in the pathogenesis of neurodegenerative diseases

Verkhratsky, Alexei, Parpura, Vladimir, Pekna, Marcela, Pekny, Milos, Sofroniew, Michael·2014·Biochemical Society Transactions
DOI 10.1042/bst20140107
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Abstract

Exclusively neuron-centric approaches to neuropathological mechanisms have not resulted in major new breakthroughs in the prevention and therapy of neurodegenerative diseases. In the present paper, we review the role of glia in neurodegeneration in an attempt to identify novel targets that could be used to develop much-needed strategies for the containment and cure of neurodegenerative disorders. We discuss this in the context of glial roles in the homoeostasis and defence of the brain. We consider the mounting evidence supporting a change away from the perception of reactive glial responses merely as secondary detrimental processes that exacerbate the course of neurological disorders, in favour of an emerging contemporary view of glial pathological responses as complex and multistaged defensive processes that also have the potential for dysfunction.

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  • Glial cells respond to nearly all types of central nervous system insults or neurodegenerative diseases, including AD, with reactive gliosis ranging from upregulation of gene transcription to enhanced secretion of matricellular proteins for remodeling of extracellular matrix surrounding neurons.

    “Glial cells respond to nearly all types of central nervous system (CNS) insults or neurodegenerative diseases, including AD.These glial responses, so called”

    From Differential protective effects of connective tissue growth factor against Aβ neurotoxicity on neurons and glia (2017) · cites this paper as [9]

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Metadata

Authors
Verkhratsky, A., Parpura, V., Pekna, M., Pekny, M., & Sofroniew, M.
Affiliations
  • Faculty of Life Sciences, The University of Manchester, Manchester M13 9PT, U.K.
  • Department of Neurobiology, Center for Glial Biology in Medicine, Atomic Force Microscopy & Nanotechnology Laboratories, Civitan International Research Center, Evelyn F. McKnight Brain Institute, University of Alabama, Birmingham, AL 35294, U.S.A.
  • Center for Brain Repair and Rehabilitation, Department of Clinical Neuroscience and Rehabilitation, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, SE-405 30 Gothenburg, Sweden
  • Department of Neurobiology, University of California, Los Angeles, CA 90095, U.S.A.
Venue
Biochemical Society Transactions
Publisher
Portland Press Ltd.
Published
2014-09-18
Volume
42
Issue
5
Pages
1291-1301
ISSN
  • 0300-5127
  • 1470-8752
DOI
10.1042/bst20140107
Cited by
141
References
31
Language
en

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